Evidence map›Paper›PMID 21228162›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Location and function of the slow afterhyperpolarization channels in the basolateral amygdala.

John M Power, Christina Bocklisch, Peter Curby, Pankaj Sah

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Mitochondrial CaCommunications biology · 2022
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  9. NPYThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
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  14. Distinct effects of repeated restraint stress on basolateral amygdala neuronal membrane properties in resilient adolescent and adult rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014
    Article
  15. Review
  16. Assignment of model amygdala neurons to the fear memory trace depends on competitive synaptic interactions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  17. Article
  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

John M PowerThe Queensland Brain Institute, The University of Queensland, Brisbane, Queensland, 4072, Australia. john.power@uq.edu.au
Christina Bocklisch
Peter Curby
Pankaj Sah
University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The basolateral amygdala (BLA) assigns emotional significance to sensory stimuli. This association results in a change in the output (action potentials) of BLA projection neurons in response to the stimulus. Neuronal output is controlled by the intrinsic excitability of the neuron. A major determinant of intrinsic excitability in these neurons is the slow afterhyperpolarization (sAHP) that follows action potential (AP) trains and produces spike-frequency adaptation. The sAHP is mediated by a slow calcium-activated potassium current (sI(AHP)), but little is known about the channels that underlie this current. Here, using whole-cell patch-clamp recordings and high-speed calcium imaging from rat BLA projection neurons, we examined the location and function of these channels. We determined the location of the sI(AHP) by applying a hyperpolarizing voltage step during the sI(AHP) and measuring the time needed for the current to adapt to the new command potential, a function of its electrotonic distance from the somatic recording electrode. Channel location was also probed by focally uncaging calcium using a UV laser. Both methodologies indicated that, in BLA neurons, the sI(AHP) is primarily located in the dendritic tree. EPSPs recorded at the soma were smaller, decayed faster, and showed less summation during the sAHP. Adrenergic stimulation and buffering calcium reduced the sAHP and the attenuation of the EPSP during the sAHP. The sAHP also modulated the AP in the dendrite, reducing the calcium response evoked by a single AP. Thus, in addition to mediating spike-frequency adaptation, the sI(AHP) modulates communication between the soma and the dendrite.

Indexed as

Action PotentialsAmygdalaAnimalsCalciumComputer SimulationDendritesExcitatory Postsynaptic PotentialsModels, NeurologicalNeuronsPatch-Clamp TechniquesPotassium Channels, Calcium-ActivatedRatsRats, WistarSynapsesCalciumPotassium Channels, Calcium-Activated

Identifiers

PMID21228162
PMCPMC6623441
OpenAlexW2064405575

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.